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J. Biol. Chem., Vol. 278, Issue 14, 11954-11961, April 4, 2003

This Article Full Text Full Text (PDF) All Versions of this Article: 278/14/11954    most recent M205329200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Whiteman, S. C. Articles by Spiteri, M. A. Search for Related Content PubMed PubMed Citation Articles by Whiteman, S. C. Articles by Spiteri, M. A. Social Bookmarking                      What's this?

Human Rhinovirus Selectively Modulates Membranous and Soluble Forms of Its Intercellular Adhesion Molecule-1 (ICAM-1) Receptor to Promote Epithelial Cell Infectivity^*

Suzanne C. Whiteman, Andrea Bianco, Richard A. Knight^§, and Monica A. Spiteri

From the Lung Injury and Inflammation Research, Directorate of Respiratory Medicine, North Staffordshire Hospital Trust, Stoke-on-Trent ST4 6QG, United Kingdom and the ^§ Department of Cystic Fibrosis, School of Medicine, Imperial College, London SW3 64R, United Kingdom

Human rhinoviruses are responsible for many upper respiratory tract infections. 90% of rhinoviruses utilize intercellular adhesion molecule-1 (ICAM-1) as their cellular receptor, which also plays a critical role in recruitment of immune effector cells. Two forms of this receptor exist; membrane-bound (mICAM-1) and soluble ICAM-1 (sICAM-1). The soluble receptor may be produced independently from the membrane-bound form or it may be the product of proteolytic cleavage of mICAM-1. The ratio of airway epithelial cell expression of mICAM-1 to the sICAM-1 form may influence cell infectivity and outcome of rhinovirus infection. We therefore investigated the effect of rhinovirus on expression of both ICAM-1 receptors in normal human bronchial epithelial cells. We observed separate distinct messenger RNA transcripts coding for mICAM-1 and sICAM-1 in these cells, which were modulated by virus. Rhinovirus induced mICAM-1 expression on epithelial cells while simultaneously down-regulating sICAM-1 release, with consequent increase in target cell infectivity. The role of protein tyrosine kinases was investigated as a potential mechanistic pathway. Rhinovirus infection induced rapid phosphorylation of intracellular tyrosine kinase, which may be critical in up-regulation of mICAM-1. Elucidation of the underlying molecular mechanisms involved in differential modulation of both ICAM-1 receptors may lead to novel therapeutic strategies.

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